Vestibular ataxia symptoms. Vestibular ataxia: the human statokinetic apparatus suffers

Vestibular ataxia is pathological condition, in which coordination of movements and the ability to maintain balance in a certain position are impaired due to a violation of the structure vestibular apparatus. A person with this symptom cannot maintain stability while sitting, standing, or walking. In addition, he may experience other signs of damage - nausea, vomiting, nystagmus, abnormalities in the functioning of the autonomic system. nervous system.

Since damage to the vestibular apparatus develops as a sign of another pathological process, then for an objective diagnosis it is necessary to take into account the symptoms of the disease that formed the basis for the manifestation of vestibular ataxia.

How does this condition arise?

Any level of dysfunction of the vestibular apparatus (cortical center of the temporal lobe of the brain, brainstem nuclei, vestibular nerve) can lead to the development of this pathology. Changes in these structures usually occur in the following diseases:

  • inflammation inner ear(labyrinthitis) with a violation of the structure of hair cells;
  • skull injuries;
  • transition inflammatory process for acute or chronic otitis media;
  • ear tumor with invasive growth;
  • toxic effect of auricular cholesteatoma;
  • Meniere's disease (characterized by paroxysmal vestibular attacks);
  • toxic effect of drugs;
  • viral infection;
  • encephalitis, arachnoiditis;
  • chronic cerebral ischemia or stroke;
  • hypertension;
  • vascular atherosclerosis or aneurysm;
  • circulatory disorders in the vertebral or labyrinthine arteries.

Symptoms accompanying vestibular ataxia

There are static (while standing) and dynamic (while walking) vestibular ataxia. Very characteristic feature, which distinguishes it from other types of ataxia, is increased instability during circular movements of the head or torso. Therefore, the patient tries to avoid pronounced movements and does this extremely slowly. Manifestations of symptoms intensify in the absence of visual control of movement.

Almost always, one side of the vestibular apparatus is affected, and the patient’s body deviates when moving in this direction. Also with this symptom, nystagmus may occur. Muscle strength and proprioceptive sensitivity in vestibular ataxia are preserved in normal volume. Sometimes there is a decrease or loss of hearing. Patients with Meniere's disease often complain of ringing in the ears.

Another one characteristic for such a pathology - the presence of systemic dizziness. It manifests itself in some patients even in horizontal position and with eyes closed. This leads to difficulty falling asleep and sleep disorders. Vestibulo-visceral connections with damage to the vestibular apparatus provoke nausea and vomiting, and a reaction in the form of redness is noted from the autonomic nervous system skin, rhythm disturbances or tachycardia, increased sweating, abrupt pressure fluctuations.

How to treat vestibular ataxia

Since vestibular ataxia is not independent disease, but only a symptom, then all efforts should be made to eliminate or relieve the severity of the underlying disease.

Inflammatory processes of the middle or inner ear are controlled by prescription antibacterial drugs, washing, sanitizing, or surgical removal purulent foci.

If the cause is a tumor process, then taking action consists of determining the exact location and type of formation. If it is possible to remove it, surgery is performed. In another case, palliative measures are used to limit its further spread.

Violation vascular circulation can be treated with numerous drug options that improve rheological properties blood, lowering cholesterol levels, stabilizing blood pressure.

Craniovertebral anomalies also often require radical surgical intervention- labyrinthectomy. It is performed in the most extreme cases, as it leads to complete deafness.

For Meniere's disease, diuretics, sedatives, a diet with a decrease in the amount of salt, abstinence from alcohol and drinks with high content caffeine The endolymphatic sac is drained and labyrinthine tissue is chemically ablated using ototoxic antibiotics. During an attack, antihistamines are used.

Symptomatic treatment for vestibular ataxia is aimed at improving cerebral circulation with the help of nootropics, B vitamins. For severe nausea, antiemetics are used. Exercise therapy plays a significant role, which helps improve coordination and strengthen muscles.

Ataxia(from the Greek ataxia - disorder) - disorder of coordination of movements; a very common motor disorder. Strength in the limbs is slightly reduced or completely preserved. Movements become inaccurate, awkward, their continuity and consistency are disrupted, balance in a standing position and when walking is disturbed. Static ataxia is a violation of balance in a standing position, dynamic ataxia is a violation of coordination when moving. Diagnosis of ataxia includes a neurological examination, EEG, EMG, MRI of the brain, and if the hereditary nature of the disease is suspected, DNA analysis. Therapy and prognosis for the development of ataxia depend on the cause of its occurrence.

General information

Ataxia(from the Greek ataxia - disorder) - disorder of coordination of movements; a very common motor disorder. Strength in the limbs is slightly reduced or completely preserved. Movements become inaccurate, awkward, their continuity and consistency are disrupted, balance in a standing position and when walking is disturbed. Static ataxia is a violation of balance in a standing position, dynamic ataxia is a violation of coordination when moving.

Normal coordination of movements is possible only with highly automated and cooperative activity of a number of parts of the central nervous system - conductors of deep muscle sensitivity, the vestibular apparatus, the temporal and frontal areas and the cerebellum - the central organ of movement coordination.

Classification of ataxias

Symptoms of ataxia

Emergence sensitive ataxia caused by damage to the posterior columns (gaulle and Burdach bundles), less often the posterior nerves, peripheral nodes, parietal cortex, thalamus opticum (funicular myelosis, tabes dorsalis, vascular disorders). It may manifest itself in all limbs, or in one leg or arm. The most indicative phenomena are sensory ataxia, which occurs as a result of a disorder of the joint-muscular sense in lower limbs. The patient is unstable, when walking he bends his legs excessively at the hip and knee joints, steps too hard on the floor (stamping gait). Often there is a feeling of walking on cotton wool or carpet. Patients try to compensate for the disorder motor functions with the help of vision - when walking, they constantly look at their feet. This can significantly reduce the manifestations of ataxia, and closing the eyes, on the contrary, aggravates them. Severe lesions of the posterior columns practically make it impossible to stand and walk.

Cerebellar ataxia - a consequence of damage to the cerebellar vermis, its hemispheres and peduncles. In the Romberg position and when walking, the patient falls (even to the point of falling) towards the affected cerebellar hemisphere. If the cerebellar vermis is damaged, it is possible to fall to any side or backward. The patient staggers when walking and places his legs wide. The flanking gait is severely impaired. Movements are sweeping, slow and awkward (more so on the part of the affected cerebellar hemisphere). Coordination disorder is almost invariable during visual control (open and closed eyes). There is a disturbance in speech - it slows down, becomes stretched, jerky, and often chanted. Handwriting becomes splayed, uneven, and macrography is observed. Possible downgrade muscle tone(more on the affected side), as well as impaired tendon reflexes. Cerebellar ataxia may be a symptom of encephalitis of various etiologies, multiple sclerosis, malignant neoplasm, vascular lesion in the brainstem or cerebellum.

Development cortical ataxia(frontal) is caused by damage to the frontal lobe of the brain caused by dysfunction of the fronto-pontine-cerebellar system. In frontal ataxia, the leg contralateral to the affected cerebellar hemisphere is most affected. When walking, there is instability (more so when turning), tilting or leaning to the side ipsilateral to the affected hemisphere. With severe lesions of the frontal lobe, patients cannot walk or stand at all. Vision control has no effect on the severity of walking disorders. Cortical ataxia is also characterized by other symptoms characteristic of damage to the frontal lobe - grasping reflex, mental changes, impaired sense of smell. The symptom complex of frontal ataxia is very similar to cerebellar ataxia. The main difference between cerebellar lesions is evidence of hypotonia in the ataxic limb. The causes of frontal ataxia are abscesses, tumors, and cerebrovascular accidents.

Hereditary Cerebellar Pierre-Marie ataxia- a hereditary disease of a chronic progressive nature. It is transmitted in an autosomal dominant manner. Its main manifestation is cerebellar ataxia. The pathogen has high penetrance, skipping generations is very rare. A characteristic pathological sign of Pierre-Marie ataxia is cerebellar hypoplasia, less often - atrophy of the inferior olives, the pons (pons). Often these signs are combined with combined degeneration spinal systems(the clinical picture resembles Friedreich's spinocerebellar ataxia).

The average age of onset is 35 years when gait disturbance appears. Subsequently, it is accompanied by disturbances in facial expressions, speech and ataxia in the hands. Static ataxia, adiadochokinesis, and dysmetria are observed. Tendon reflexes are increased (to pathological reflexes). Involuntary muscle twitches are possible. Strength in the muscles of the limbs is reduced. Progressive oculomotor disorders are observed - paresis of the abducens nerve, ptosis, convergence insufficiency, less often - Argyll Robertson's symptom, optic nerve atrophy, decreased visual acuity, narrowing of visual fields. Mental disorders manifest themselves in the form of depression, decreased intelligence.

Familial Friedreich's ataxia- a hereditary disease of a chronic progressive nature. It is transmitted in an autosomal dominant manner. Its main manifestation is mixed sensory-cerebellar ataxia, resulting from combined lesion spinal systems. Consanguineous marriages are very common among patients' parents. A characteristic pathological sign of Friedreich's ataxia is increasing degeneration of the lateral and posterior columns spinal cord(before medulla oblongata). Gaulle's bundles are most affected. In addition, the cells of Clark's columns are affected, and along with them the posterior spinocerebellar tract.

The main symptom of Friedreich's ataxia is ataxia, expressed in an uncertain, clumsy gait. The patient walks in a sweeping manner, deviating from the center to the sides and placing his feet wide. Charcot designated this gait as a tabetic-cerebellar gait. As the disease progresses, incoordination spreads to the arms and muscles. chest and face. Facial expressions change, speech becomes slow and jerky. Tendon and periosteal reflexes are significantly reduced or absent (primarily on the legs, then on upper limbs). In most cases, hearing is reduced.

With the development of Friedreich's ataxia, extraneural disorders appear - cardiac lesions and skeletal changes. The ECG shows deformation of the atrial wave, rhythm disturbance. There is paroxysmal pain in the heart, tachycardia, shortness of breath (as a result physical stress). Skeletal changes are expressed in characteristic change foot shape - a tendency to frequent joint dislocations, increased arches and extension of the toes, as well as kyphoscoliosis. Among the endocrine disorders accompanying Friedreich's ataxia are diabetes, hypogonadism, and infantilism.

Ataxia-telangiectasia(Louis-Bar syndrome) is a hereditary disease (phakomatoses group), transmitted in an autosomal recessive manner. Very often accompanied by dysgammaglobulinemia and hypoplasia thymus gland. The development of the disease begins early childhood when the first ataxic disorders appear. In the future, ataxia progresses and by the age of 10, walking is almost impossible. Louis-Bar syndrome is often accompanied by extrapyramidal symptoms (hyperkinesis of the myoclonic and athetoid type, hypokinesia), mental retardation, defeat cranial nerves. Characterized by a tendency to repeated infections(rhinitis, sinusitis, bronchitis, pneumonia), which is primarily due to the insufficiency of the body’s immunological reactions. Due to the deficiency of T-dependent lymphocytes and class A immunoglobulins, there is a high risk of developing malignant neoplasms.

Complications of ataxia

Diagnosis of ataxia

Diagnosis of ataxia is based on identification of diseases in the patient's family and the presence of ataxia. EEG of the brain in Pierre Marie's ataxia and Friedreich's ataxia reveals the following disorders: diffuse delta and theta activity, reduction of the alpha rhythm. IN laboratory research there is a disturbance in amino acid metabolism (the concentration of leucine and alanine is reduced, and their excretion in the urine is also reduced). MRI of the brain reveals atrophy of the spinal cord and brain stems, as well as upper sections worm. Using electromyography, axonal demyelinating damage to the sensory fibers of peripheral nerves is detected.

When differentiating ataxia, it is necessary to take into account variability clinical picture ataxia. IN clinical practice rudimentary varieties of ataxia and its transitional forms are observed when clinical manifestations similar to symptoms of familial paraplegia (spastic), neural amyotrophy and multiple sclerosis.

To diagnose hereditary ataxias, direct or indirect DNA diagnostics is necessary. Using molecular genetic methods, ataxia is diagnosed in a patient, after which indirect DNA diagnostics are performed. With its help, the possibility of inheriting the ataxia pathogen by other children in the family is established. It is possible to carry out complex DNA diagnostics; it will require biomaterial from all family members (the child’s biological parents and all other children of this parental couple). In rare cases, prenatal DNA diagnosis is indicated.

Treatment and prognosis of ataxia

Ataxia is treated by a neurologist. It is predominantly symptomatic and should include: restorative therapy (B vitamins, ATP, anticholinesterase drugs); special complex gymnastic exercises Exercise therapy aimed at strengthening muscles and reducing incoordination. With Friedreich's ataxia, taking into account the pathogenesis of the disease, drugs that support mitochondrial functions can play a major role in treatment ( succinic acid, riboflavin, coenzyme Q10, vitamin E).

To treat ataxia-telangiectasia, in addition to the above algorithms, correction of immunodeficiency is necessary. For this purpose, a course of treatment with immunoglobulin is prescribed. Radiation therapy in such cases it is contraindicated; in addition, excessive x-ray radiation and prolonged exposure to the sun should be avoided.

The prognosis of genomic hereditary diseases is unfavorable. There is a slow progression of neuropsychiatric disorders. Working capacity in most cases is reduced. However, through symptomatic treatment and prevention of recurrent infectious diseases, injuries and intoxications, patients have the opportunity to live to an old age. For preventive purposes, the birth of children in families where there are patients should be avoided. hereditary ataxia. In addition, it is recommended to exclude the possibility of any related marriages.

Occurs when the functions of the vestibular analyzer, in particular its proprioceptors in the labyrinth, are impaired. Occurs with damage to the vestibular apparatus (semicircular canals, ampullae), with vestibulopathies, with Meniere's syndrome, Meniere's disease, with neuroma of the auditory portion of the VIII pair, with vascular diseases accompanied by the appearance of a lesion in the area of ​​the vestibular nuclei of the trunk, with vertebrobasilar insufficiency, SPA.

With vestibular ataxia, the balance of the body is upset, the patient deviates when walking and in the Romberg position towards the affected labyrinth. The severity of ataxia increases with changes in the position of the body and head.

Characteristic:

      systemic dizziness;

      horizontal rotatory nystagmus;

      nausea, vomiting;

      on the side of the affected labyrinth, hearing may decrease (if the auditory portion of the VIII pair is involved in the process).

Relief of vestibular crisis:

Cerucal 2.0

Diazepam 2.0

Atropine 0.1-0.5%

If blood flow in the labyrinthine artery is impaired, a drug is used that selectively improves blood flow in this artery - betaserc. Also, in the treatment of chronic cerebrovascular accident, or stroke, accompanied by vestibular disorders, antidepressants and diuretics are used; Eglonil is used for emotional disorders. For chronic dizziness of labyrinthine origin, exercise therapy is of great importance.

Cerebellum and vestibular system (anatomy and physiology).

Cerebellar ataxia develops not only when the cerebellum itself is damaged, but also its conductors; both afferent and efferent. Closing the eyes does not affect cerebellar ataxia; deep sensitivity remains intact.

The cerebellum is located in the posterior cranial fossa above the medulla oblongata and the pons. Above it are the occipital lobes, between them and the cerebellum the cerebellar tentorium is stretched. The cerebellum consists of the middle section or vermis and two hemispheres. The superficial layer of the cerebellum is the cortex - gray matter. In addition, in the white matter there are also accumulations of gray matter - the cerebellar nuclei. The most important of them are nucl. dentatus (dentate nucleus), nucl. fastigi - the core of the tent.

The cerebellum is connected to other parts of the central nervous system by three pairs of peduncles:

1) lower legs - corpora restiformia (rope bodies) (connect the cerebellum with the medulla oblongata);

2) middle legs - brachia pontis (connect the cerebellum with the pons);

3) upper legs - brachia conjunktiva (connect the cerebellum with the midbrain at the level of the quadrigeminal).

The cerebellar peduncles consist of fibers that carry impulses to or away from the cerebellum.

The cerebellar vermis is a phylogenetically more ancient section associated with the vestibular apparatus.

The cerebellar hemispheres are a newer formation, developing in parallel with the development of the cerebral cortex.

The cerebellum does the following functions :

    automatic coordination of movements;

    regulation of muscle tone;

    ensuring body balance.

In the implementation of voluntary movements, the main role of the cerebellum is to coordinate the fast (phasic) and slow (tonic) components of the motor act. This is possible due to the connections of the cerebellum with the muscles and cerebral cortex.

The cerebellum receives afferent impulses from all receptors that are stimulated during movement - these are proprioceptors, vestibular, visual, auditory, i.e. receives information about the state of the motor system.

The cerebellum itself influences the red nucleus and the reticular formation of the brainstem, which send impulses to the γ-motoneurons of the spinal cord, which regulate muscle tone. Impulses from the cerebellum enter the motor cortex. The main function of the cerebellum is carried out at the subcortical level: brain stem, spinal cord.

Efferent impulses from the cerebellar nuclei regulate proprioceptive stretch reflexes. During muscle contraction, proprioceptors (muscle spindles) are excited in the agonist and antagonist muscles, but the reflex does not occur, since the cerebellum has an inhibitory effect. When the cerebellum is damaged, this influence is lost, and oscillatory movements appear in the limbs when performing movements (especially when performing purposeful actions due to the excitation of agonists and antagonists). Many cerebellar disorders are associated with a violation of the reciprocal innervation of antagonists: when performing any muscle movement, the agonists and antagonists are in the opposite state. If the flexor neurons are excited, the extensor neurons are inhibited. The mechanism consists of reciprocal inhibition of spinal motor centers. This mechanism is carried out by the segmental apparatus of the spinal cord with the participation of the cerebellar systems.


Vestibular ataxia is a syndrome that occurs when a special part of the brain is damaged, which is often referred to as the small central organ. In addition, the cerebellum includes its own small hemispheres, as well as various substances. The gray ones form the cortex, and the white ones form the nervous structures that make up it.

The fibers contain nerve nuclei that play a huge role in conducting impulses that ensure the cerebellum performs the following group of functions:

  • Coordination of movements, smoothness of their act and proportionality;
  • Maintaining body balance in space;
  • Regulation of muscle tone, its redistribution and maintenance, which allows you to adequately perform the functions assigned to the muscles;
  • Formation of a center of gravity in the body;
  • Synchronization of movements;
  • Anti-gravity force that keeps a person on the ground.

The cerebellum itself is located in the posterior fossa of the skull and weighs about 130 g. It is about 10 cm long and about 5 cm wide. Such a small organ performs functions that are extremely important for human existence. When its functioning is disrupted, a condition called vestibular ataxia occurs. There are many types of ataxic disorders: frontal, trunk, sensory. However, those associated with the cerebellum are called vestibular or cerebellar.

Ataxia is characterized by a disorder of coordination and motor skills. This disrupts the motor act, a person’s gait and his balance in space. In addition to the main ones, it is characterized by a number of specific symptoms and is accompanied by a group of signs.

Types of ataxia

Basic forms:

  • Static-locomotor, which appears in a stationary position and is caused by damage to the cerebellar vermis;
  • Dynamic, manifested during human movement and associated with the destruction of the hemispheres and its connections.

According to the nature of the course, vestibular ataxia can be:

  • With acute or subacute onset, which lasts from 7 days to a couple of weeks;
  • With chronic progression that develops over several months or years;
  • Episodic, which is sometimes called paroxysmal.

Ataxia can be caused by many causal factors. The main list includes:

  • Ischemic or hemorrhagic stroke;
  • Transient attacks;
  • Discirculatory encephalopathy;
  • Multiple sclerosis;
  • Tumor formations;
  • Traumatic brain injury associated with damage to the cerebellum;
  • Infectious diseases - meningitis or meningoencephalitis;
  • Degenerative disorders of the nervous system that damage the cerebellum and lead to Friedreich's ataxia or Arnold-Chiari malformation;
  • Intoxication caused by drinking alcohol or narcotic substances, medicines, for example, anticonvulsants, toxic effects of lead;
  • Metabolic disorders caused by diabetes mellitus;
  • Vitamin B12 deficiency;
  • Obstructive hydrocephalus.

Signs

Cerebellar ataxia and the types that occur have their own special features. They are specific in nature and are immediately noticeable when looking at the patient. The appearance of signs is quite difficult to miss. And although there are special symptoms, general signs forms of the disease have:

  • The presence of sweeping, uncertain, uncoordinated movements that tend to fall;
  • Unsteadiness of gait, in which people stand unsteadily on their feet, balance with their arms, and spread their feet wide for greater stability;
  • Unplanned stops earlier than planned;
  • Increased motor amplitude;
  • Inability to stand upright;
  • Involuntary rocking;
  • Intention tremor, manifested as absence at rest and intense trembling of the limbs during movement;
  • Nystagmus, characterized by involuntary twitching of the eyeballs;
  • Adiadochokinesis, manifested by the patient’s lack of ability to perform motor acts with alternation. Such people do not tend to quickly perform tasks like “unscrewing a light bulb.” At the same time, the movement of their hands is not coordinated;
  • A handwriting disorder that manifests itself as uneven, splayed, and large writing;
  • Dysarthria associated with speech impairment, in which it loses its smoothness and slows down, large pauses appear between words and sounds like intermittent and chanted sounds, with emphasis on each syllable;
  • Muscle hypotonicity associated with decreased tone and inhibition of deep reflexes.

Locomotor ataxia is characterized by a number of symptoms:

  • Inability to stand straight;
  • Falling forward or backward, as well as swaying;
  • By spreading your legs wide and balancing your arms so as not to fall;
  • Unsteady gait, as if drunk.

Dynamic ataxia manifests itself:

  • Intention tremor in the limbs;
  • Missing and missing caused by disproportionate muscle contraction. In view of this, it becomes impossible for patients to do the simplest and most common things - bring a spoon to the mouth or fasten a button;
  • Impaired handwriting;
  • Scanned speech;
  • Nystagmus;
  • Adiadochokinesis;
  • Pendulum-like knee-jerk reflexes.

Diagnosis and treatment of ataxic lesions

The study of ataxia is not difficult. During the examination, the neurologist performs functional tests to assess the patient's condition. To identify static ataxia, the following tests are performed:

  • In the Romberg position, in which the patient is asked to stand straight and extend his arms forward. The patient is tested first with with open eyes, or closed. The static type of ataxia leads to the fact that a person becomes unstable. He cannot stand straight;
  • Walking in a straight line, which is impossible in conditions of ataxia. Patients will deviate to one side, while spreading their legs wide apart. Such attempts to walk straight are often accompanied by falls;
  • Walking with an extended step, which is impossible in conditions of ataxia. The person dances, while the body lags behind the limbs.

To identify the dynamic type of ataxia, the following types of tests are performed:

  • Finger-nasal, during which the patient is asked to put his finger in his own nose, performed with open and closed eyes. In conditions of dynamic vestibular ataxia, the finger falls past the nose, and, approaching it, experiences an intention tremor;
  • Finger hammer, similar to the previous one, except that the patient is asked to hit the doctor’s neurological hammer with his finger. Patients with ataxia miss;
  • Heel-knee, which is performed on the back. Legs extended. The patient’s heel should hit the other’s knee and “ride” down the front surface of the shin to the foot. Then they are asked to repeat a similar movement with the other leg. Patients with dynamic ataxia cannot perform this action fully. They either do not hit the knee with the heel, or cannot slide smoothly along the leg.

Due to the wide range of causative factors of ataxia, there is no single plan for its treatment, since this is a manifestation of some disease. Therefore, they treat the root cause directly. Conduct symptomatic treatment the following group of drugs:

  • Betahistine and its derivatives - Betaserc or Vestibo;
  • Nootropics and antioxidants, such as Piracetam or Phenotropil, Phenibut or Cytoflavin, Cerebrolysin and Actovegin;
  • Improving blood flow - Cavinton or Pentoxifylline;
  • B vitamins and their complexes like Milgamma or Neurobex;
  • Increasing muscle tone - Mydocalm and Baclofen;
  • Anticonvulsants such as carbamazepine or pregabalin.

Vestibular ataxia is not a death sentence at all. Its signs are immediately noticeable, so you can notice the symptoms quite quickly. This means that contacting a doctor should be timely. The earlier the type of ataxia is diagnosed, be it cortical or vestibular ataxia, the greater the likelihood of providing full assistance to the patient.

Video

Vestibular ataxia (labyrinthine) is a violation of coordination of movements and gait, which is associated with disruption of the vestibular apparatus. Accompanied by the presence of nystagmus, systemic dizziness, nausea and vomiting. Autonomic abnormalities may occur (tachycardia, pallor or redness of the face, increased sweating).

Since ataxia is not an independent disease, but a symptom of other diseases (develops against the background of traumatic brain injury, etc.), vestibular ataxia is also characterized by signs of the underlying, primary disease.

General information

Ataxia – Greek word, which translates as “confusion”, “disorder”. It has been used as a medical term since the time of Hippocrates.

Systemic dizziness - often found in medical practice a symptom that almost always accompanies vestibular ataxia. It is systemic dizziness that is often the reason for visiting neurologists (10% of all cases) and otolaryngologists (about 4% of all cases).

Labyrinthine ataxia is one of the main causes of falls and subsequent injuries in old age.

Forms

Depending on the nature of the manifested violations, the following are distinguished:

  • static vestibular ataxia, which manifests itself in a standing position;
  • dynamic vestibular ataxia, in which symptoms manifest themselves in movement.

It is usually unilateral, but a bilateral form is also found.

Reasons for development

Vestibular ataxia occurs when the structures of the vestibular apparatus are damaged at any of its levels (labyrinth, vestibular nerve (VIII pair), nuclei located in the brain stem, vestibular analyzer cortical center in the temporal lobe).

Pathology can occur when:

  • Damage to the hair cells that are located inside the membranous labyrinth (inner ear).
  • Ear injuries that are accompanied by damage to the labyrinth. More often there are injuries in which neighboring organs are also damaged (combined injuries).
  • Inflammatory processes of the middle ear, which are accompanied by the spread of infection to the labyrinth (acute and chronic purulent otitis media).
  • New growths of the ear, which are characterized by penetration through tissue tumor cells(invasive type of growth).
  • Meniere's disease. This disease of the inner ear is characterized by the presence in the ear cavity of an increased amount of endolymph, which puts pressure on the cells responsible for balance. Labyrinthine ataxia in this case is paroxysmal in nature.
  • Rarely occurring tumor, infectious (herpes, ARVI) or toxic damage to the vestibular nerve.
  • Traumatic brain injuries leading to damage to the vestibular nuclei, which are located in the rhomboid fossa (the bottom of the fourth ventricle, formed by the bridge and the posterior surface of the medulla oblongata).
  • Pathologies of the craniovertebral region (atlas assimilation, platybasia), causing compression of the medulla oblongata. Compression also causes the formation of a tumor on the brain stem.
  • Blood flow disorders in atherosclerosis, increased blood pressure, aneurysms of cerebral vessels, which lead to ischemia of the brain stem.

Encephalitis, multiple sclerosis, acute encephalomyelitis and posterior arachnoiditis cranial fossa also contribute to the development of vestibular ataxia.

Pathogenesis

Orientation human body in space is provided by the vestibular analyzer. It is thanks to the vestibular analyzer that the perception of gravity, the position and nature of the movement of body parts and the movement of the body in space are determined.

Every change in body position is perceived by hair cells - vestibular receptors, which are located on the thin basilar membrane in the receptor part auditory analyzer(inside the anterior part of the membranous labyrinth).

Hair cells transmit impulses along the vestibular nerve (belongs to the VIII pair of cranial nerves) to the vestibular nuclei, which are responsible for the synthesis of information.

Control of motor reactions is carried out due to the transmission of regulatory nerve impulses from the vestibular nuclei to various departments The central nervous system, which ensures the maintenance of balance and redistribution of muscle tone due to reflex reactions.

Defeat any part vestibular analyzer causes imbalance and coordination of movements.

Symptoms

Vestibular ataxia differs from other forms of this disorder:

  • dependence of the severity of symptoms on movements and turns of the head and body;
  • severe disturbances in walking and standing without involving the limbs and speech disorders.

Vestibular ataxia is characterized by the presence of:

  • Systemic severe dizziness, which may be present even in a supine position. Often accompanied by nausea and vomiting.
  • Horizontal nystagmus (involuntary oscillatory movements of the eyes along a horizontal line, which differ high frequency), which, with a unilateral lesion, is directed to the side opposite the affected area. Damage to the vestibular nuclei is accompanied by vertical (usually asymmetric) nystagmus with a rotation component. When vestibular connections are disrupted, bilateral nystagmus may occur.
  • Staggering when walking (tendency to fall), in which there is a deviation towards the existing lesion. Deviation to the affected side is also observed in a sitting or standing position.

Possible hearing loss. Coordination of hand movements is preserved.

Symptoms that intensify when turning the head, body or eyes force the patient to perform these movements very slowly and try in every possible way to avoid them. Visual control largely compensates for impaired coordination, so with closed eyes a person does not feel confident, and symptoms progress.

There are no violations of muscle-articular sensation.

If you experience dizziness while lying down with your eyes closed, sleep disturbances (difficulty falling asleep) are often present.

Vegetative reactions may also occur:

  • pale or red face;
  • feeling of fear;
  • tachycardia;
  • pulse lability;

Diagnostics

The diagnosis of vestibular ataxia is based on:

  • Anamnesis data. The doctor clarifies when the first symptoms of the disease appeared, what the patient suffered from during his life, what hereditary diseases were in the family.
  • Data general examination. The examination includes assessment of reflexes and muscle tone, hearing and vision, and coordination tests. A “star test” is performed, in which the patient with his eyes closed tries to take several steps in a straight line, but at the same time the trajectory of his movement with ataxia is similar to a star, Romberg’s pose is assessed (feet in a standing position are moved together, eyes are closed, arms are extended straight in front of him ) etc.
  • Data from laboratory and instrumental studies.

To determine the type of ataxia and identify the nature and level of damage to the vestibular analyzer, the following is carried out:

  • X-ray studies that reveal craniovertebral anomaly. The skull and spine in the cervical region are examined.
  • REG. This study is carried out to obtain indirect data on blood circulation in the brain. If there is a need to examine in detail the blood circulation of the cerebral vessels, angiography or MRI angiography is performed.
  • Echo-EG, which allows you to assess the state of the liquor system. If the echo is displaced, we can conclude that there is a tumor, abscess or hematoma in the brain, which can provoke vestibular ataxia.
  • EEG, which helps evaluate bioelectrical activity brain
  • CT and MRI to detect volumetric formations and the presence of demyelinating processes.

The vestibular analyzer is examined by a vestibulologist (in his absence, a neurologist or otolaryngologist) using:

  • Vestibulometry, allowing to assess its functions. Includes caloric, rotational, index, finger-nose and pressor tests, Vojacek's otolith reaction (the study begins with the finger-nose and index test).
  • Stabilography, which allows you to evaluate the vibrations of the human body while maintaining an upright posture.
  • Videooculography, which records eye movements and allows you to analyze nystagmus (disturbances of the vestibular analyzer at the peripheral level are accompanied by increased nystagmus when turning the head with a decrease in nystagmus with repeated turns, increased nystagmus when tilting the head with craniovertebral anomaly, etc.)
  • Electronystagmography, which allows you to record eye movements with closed eyelids.

To study hearing, threshold audiometry, tuning fork testing, electrocochleography, etc. are used.

Treatment

Treatment of vestibular ataxia is aimed at curing the primary disease. Includes:

  • Antibiotic therapy for infectious lesion ear. Middle ear lavage, labyrinthectomy for labyrinthitis and other measures are also carried out to eliminate the purulent focus.
  • The use of drugs that improve blood supply to the brain during vascular disorders(angioprotectors, nootropics), as well as drugs for normalizing blood pressure.
  • Reception hormonal drugs and plasmapheresis for demyelinating diseases.
  • The use of diuretics and sedatives for Meniere's disease, as well as prescribing a diet with low content salt and avoiding alcohol and caffeine. Ototoxic antibiotics (gentamicin, etc.) are used for chemical ablation (cauterization, removal) of labyrinthine tissue.
  • Surgical correction for severe craniovertebral anomalies.
  • Surgical methods in the presence of tumor or hemorrhage.

Symptomatic treatment is also carried out, including:

  • taking medications that improve function and metabolism nerve cells(ginkgo biloba, cerebrolysin, B vitamins, etc.);
  • a physical therapy complex that strengthens muscles and trains coordination of movements.

Prevention

Prevention of vestibular ataxia consists of: